The Myc regulator genes encode a family of transcription factors involved in cell proliferation, growth, differentiation and apoptosis. Members of the Myc transcription factor family include c-Myc, N-Myc and L-Myc. Myc proteins activate expression of many genes through binding of consensus sequences (Enhancer Box sequences (E-boxes)) and recruiting histone acetyltransferases. Activation of normal Myc genes affects numerous cellular processes, including cell cycle progression, cell growth and division, metabolism, telomerase activity, adhesion and motility, angiogenesis and differentiation.
Myc is also a very strong proto-oncogene and mutated versions are often found to be upregulated and/or constitutively expressed in many types of cancers. Many hematological and solid tumor malignancies have been found to possess aberrations in one or more Myc genes. The major genetic Myc aberrations found in human tumors include gene amplification in solid tumors and chromosome translocation in lymphoma and leukemia.
Myc-dependent cancers cells do not survive in the absence of Myc. Many researchers have attempted to exploit this vulnerability by developing chemotherapeutic agents targeting Myc. However, attempts at designing effective small molecule inhibitors of Myc have been unsuccessful because the proteins are small and do not provide good binding sites for chemotherapeutic agents.
Accordingly, there is a need for new classes of chemotherapeutic agents that target and efficiently downregulate Myc.